In individuals who have developed coronary disease after a life of hypercholesterolemia, it generally is too late to reverse the disease by lowering the serum cholesterol. It would be better, therefore, to lower the serum cholesterol level early in life, so to prevent the development of potentially obstructive atherosclerosis. But how early in life should unpalatable measures to reduce serum cholesterol be recommended to individuals that are still unsymptomatic? Some persisting questions about the natural history of atherosclerosis have prevented sure recommendations to the young population at large. Thus, it is uncertain whether the fatty streaks of children are an early stage of atheromas or whether atheromas develop through some other pathway. It is not clear whether one should prevent in children the evolution of fatty streaks, or whether dietary intervention should be postponed to prevent the possibly independent atheromas which, as gross autopsy evidence indicates, begin to occur at least a decade later in life. Since atheromas are probably not of a single origin, the relative incidence, and the mechanism and rate of progression of each type, should be established. To contribute this information is the aim of this study. We are investigating the coronary arteries and aortas of individuals of both sexes, black and white, aged from fullterm birth to 39 years, obtained post-mortem at the Morgue of the Coroner of new Orleans and at Charity Hospital of New Orleans. We are specifically studying the following points: changes in fatty streaks that might indicate progressive transition into the potentially obstructive atheromas and fibroatheromas, and the reason for it; the presence and frequency of thrombotic encrustations, hemorrhages or other changes on or within intima, fatty streaks, atheromas, and fibroatheromas, pointing to lesion generation or progression through these mechanisms; the influence on lesion development of individual and local variations in intima thickness (the influence on lesion generation of the degree of preexisting eccentric and diffuse intima thickening). We use light microscopy of 1-Mum plastic-embedded sections, histochemistry, and electron microscopy to identify and quantitate cells and extracellular matrix, and circulation-derived components of intima, media, adventitia and lesions. For the quantitations we use a sonic digitizer coupled to a computer. To characterize and quantitate the functional status of cells we use enzyme cytochemistry, and to determine changes in the nature of intimal lipid we use chemical lipid analysis.